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  • 1
    ISSN: 1432-2129
    Keywords: Schlüsselwörter Trigeminusneuralgie ; CSF ; Neurotransmitter ; Substanz P ; Somatostatin ; Key words Trigeminal neuralgia ; Neurotransmitters ; CSF ; Substance P ; Somatostatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract The etiology of trigeminal neuralgia is unknown, but both peripheral and central causes have been suggested. To investigate the role of central neurochemical mechanisms we measured epinephrine, norepinephrine and their breakdown product, vanilly mandelic acid (VMA), in the cerebrospinal fluid (CSF) of 16 patients (53.3 ± 8.3 years) suffering from trigeminal neuralgia. As markers for the dopaminergic system, we determined CSF levels of dopamine and its metabolite homovanillic acid (HVA). As a marker for the serotonergic system, we measured CSF levels of serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). In addition, levels of the neuropeptides substance P and somatostatin were determined. The concentration of norepinephrine (P 〈 0.01), VMA (P 〈 0.05) and HVA (P 〈 0.05) were significantly decreased in patients with trigeminal neuralgia and correlated with the duration of the disease and depression scores. 5-HIAA was also significantly decreased (P 〈 0.05) compared to control patients. Whereas substance P was significantly elevated (P 〈 0.05), somatostatin was significantly decreased (P 〈 0.05). Various correlations between the classical neurotransmitters and the neuropeptides could be established. We hypothesize than the sum of complex neurochemical changes plays a role in the etiology of trigeminal neuralgia, which can be separated in local and more central proceedings. The increase in substance P, a major nociceptive neuromodulator, supports the concept of a local neurogenic inflammation, possibly located in the trigeminovascular system. Depending on the duration of the disease and depression, the loss of serotonergic, dopaminergic and noradrenergic innervation seems to reflect more central changes, possibly due to alterations in their antinociceptive descending pathways.
    Notes: Zusammenfassung Bei der Trigeminusneuralgie werden periphere und zentrale Entstehungsmechanismen diskutiert. Daher wurden bei 16 Patienten (53,3 ± 8,3 Jahre) mit einer idiopathischen Trigeminusneuralgie in der Zerebrospinalflüssigkeit (CSF) die Neuropeptide Substanz P und Somatostatin, die Neurotransmitter Noradrenalin und Adrenalin sowie die Metaboliten Homovanillinmandelsäure (HVA), Vanillinmandelsäure (VMA) und 5-Hydroxyindoleessigsäure (5-HIAA) bestimmt. Während die Substanz P in der CSF signifikant (p 〈 0,01) erhöht gefunden wurde, war das Somatostatin gegenüber den Kontrollpersonen signifikant erniedrigt (p 〈 0,05). Noradrenalin (p 〈 0,01), 5-HIAA (p 〈 0,01), HVA (p 〈 0,05) und VMA (p 〈 0,05) waren signifikant erniedrigt. Während die Erhöhung der Substanz P einen Hinweis auf eine lokal beschränkte neurogene Entzündung im trigemino-vaskulären System geben könnte, spricht die Reduktion monoaminerger Transmitter für eine zentral gestörte Schmerzmodulation. Diese scheint mit zunehmender Krankheitsdauer und begleitender Depression stärker zu werden. Die zahlreichen Korrelationen der Neuromediatoren untereinander, insbesondere auch zwischen den Neuropeptiden und den klassischen Neurotransmittern, sprechen für komplexe neurochemische Interaktionen im Rahmen der Schmerzentstehung.
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  • 2
    ISSN: 1468-2982
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To investigate sympathetic nervous system and neuroendocrine changes in idiopathic trigeminal neuralgia, we determined the plasma level of the catecholamines norepinephrine and epinephrine, as well as cortisol and ACTH in 16 patients (55.38.3 years) with trigeminal neuralgia at four different times during the day (7.00, 13.00, 17.00 and 23.00). Morning and evening values of plasma norepinephrine as well as the daily mean value (dmv) were significantly higher (p〈0.01) in patients with trigeminal neuralgia than in an age- and gender-matched control group. Moreover, morning, afternoon and dmv epinephrine values were also significantly elevated. The dmv norepinephrine levels correlated with the intensity of the attacks (r=0.68, p〈0.01), the frequency of the attacks (r=0.75, p〈0.01) and the duration of the disease (r=0.78, p〈0.01). In addition to elevated catecholamines, trigeminal neuralgia patients also demonstrated significantly increased morning, evening and daily mean values of plasma cortisol. Thus, patients with trigeminal pain have an increased sympathetic nervous system activity for an extended period of time without a direct link to pain attacks, which suggests that the sympathetic nervous system itself is at least co-activated in trigeminal neuralgia and perhaps plays a role in the induction and maintenance of trigeminal pain. The neuroendocrine changes are similar to cluster headache and point to a central dysregulation of the hypothalamic-pituitary-adrenal axis, possibly due to the cyclic phenomena in idiopathic trigeminal neuralgia.
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  • 3
    ISSN: 1432-1459
    Keywords: Key words Paraneoplastic ; neurological syndrome ; Intravenous immunoglobulins ; Therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The treatment of paraneoplastic neurological syndromes (e.g., tumor therapy, immunosuppressive therapy, plasmapheresis) rarely leads to an improvement in the neurological symptoms. We treated four patients suffering from paraneoplastic neurological syndromes with intravenous immunoglobulins. All four had high titers of antineuronal antibodies in serum and CSF. Two of the patients, one suffering from paraneoplastic cerebellar degeneration and the other from paraneoplastic brain stem encephalitis and polyneuropathy, received intravenous immunoglobulin treatment within 3 weeks of the onset of neurological symptoms. Both patients showed clinical improvement within 2 weeks after the initiation of therapy. They also showed a decline in the intrathecal antibody synthesis of the antineuronal antibody. Two other patients, who had suffered from paraneoplastic neuropathy for 3 and 6 months showed no improvement with the intravenous immunoglobulin therapy. In these cases there was no effect on intrathecal antibody synthesis. When started early, intravenous immunoglobulins may be of therapeutical value in treating paraneoplastic neurological syndromes. Specific intrathecal antibody synthesis may be a better measure of clinical course that autoantibody serum titers.
    Type of Medium: Electronic Resource
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